We have discovered four mutants of the mouse which are visually defective because they lack the optokinetic nystagmus. These mutants have normal-sized eyes, are able to move their eyes in response to vestibular stimulation, have no gross histological abnormalities of the retina or brain, and have no grossly observable neurological disorders. Electrophysiological analysis of one of the mutants has shown that the response properties of the cells of its superior colliculus are abnormal in sevaral ways. Another one of the mutants is the animal which has been proposed as a model for human Chediak-Higashi syndrome. The proposed research will identify the place in the visual system where each mutant gene exerts its effect. This identification will be done using histology, autoradiography, and electrophysiology. There are two ultimate aims of this research: (1) to provide new animal models for hereditary human diseases and further analyze the visual system of the mutant that is a model for Chediak-Higashi syndrome, (2) to advance our basic understanding of the visual system with the analytical tool that these mutants provide.